This is a condition that usually occurs secondary to advanced liver disease and is marked by a disturbance of mental functioning. Hepatic means “of the liver” and Encephalopathy means “a disorder of the brain.”
Hepatic encephalopathy is the result of biochemical abnormalities associated with liver failure. Although disturbed ammonia metabolism is one component of hepatic encephalopathy, it is clear that ammonia is not solely responsible for the disturbed mental status.
Encephalopathy is the mandatory clinical feature for diagnosis of acute liver failure. Difficulties in the recognition of the early stages of encephalopathy and distinction from drug-induced and renal (kidney)-induced alterations of mental state do not detract from the value of this sign as the most powerful clinical indicator of the severity of liver disease.
Once encephalopathy develops, the patient is at high risk for the development of cerebral edema and multiorgan failure.
Hepatic encephalopathy may be aggravated by sepsis. Bleeding into the intestinal tract may significantly increase the amount of protein in the bowel and may precipitate rapid development of liver coma.
Other factors that may precipitate hepatic encephalopathy include alkalosis, potassium deficiency induced by diuretics, narcotics, hypnotics, and sedatives; medications containing ammonium or amino compounds; and infection of the liver or throughout the body.
There is a disturbance of consciousness that may progress to deep coma (hepatic coma), psychiatric changes of varying degree, flapping tremor, and fetor hepaticus (breath odor associated with hepatic disease).
The diagnosis is made on the basis of the medical history and physical examination including the mental status exam. Blood tests may be performed to evaluate the ammonia level.
Current clinical management of hepatic encephalopathy in acute liver failure is derived from experience in chronic liver disease. Generally accepted measures for the treatment of acute hepatic encephalopathy include correction and avoidance of any factor that could potentially aggravate pre-existent encephalopathy, such as hypoglycemia (low blood sugar), hypoxia (low oxygen), bleeding, sepsis, drug toxicity, and electrolyte and acid-base disturbance.
Lactulose and dietary protein elimination are commonly used to treat acute hepatic encephalopathy. Lactulose is a nonabsorbable synthetic sugar that acidifies ammonia in the colon and allows it to form ammonium that can be excreted. Antibiotics may be used to control bacteria growth in the colon that produce ammonia and worsen the encephalopathy.
Gastrointestinal bleeding should be controlled if possible and blood purged from the gastrointestinal tract. Blood is broken down into protein which tends to worsen the encephalopathy. This can be accomplished with magnesium citrate by mouth, or a nasogastric tube every 3 to 4 hours until the stool is free of blood.
What is the cause of the encephalopathy?
Is it drug-related?
Is there an underlying medical problem precipitating encephalopathy?
What is its relationship to acute liver failure?
What treatment do you recommend?
What is the prognosis?